ROLE OF THE RENIN-ANGIOTENSIN SYSTEM IN HYPERTENSION PRODUCED BY UNILATERAL RENAL ARTERY CONSTRICTION IN THE RAT

SUMMARY 1. Conscious rats which had undergone unilateral renal artery constriction were infused for 1 h with a specific antagonist of angiotensin II, 1‐Sar‐8‐Ala‐angiotensin II (P‐113). 2. There was a highly significant correlation between the change in blood pressure induced by P‐113 and the pre‐in...

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Veröffentlicht in:Clinical and experimental pharmacology & physiology 1976-01, Vol.3 (1), p.95-98
1. Verfasser: Oates, Helen F.
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description SUMMARY 1. Conscious rats which had undergone unilateral renal artery constriction were infused for 1 h with a specific antagonist of angiotensin II, 1‐Sar‐8‐Ala‐angiotensin II (P‐113). 2. There was a highly significant correlation between the change in blood pressure induced by P‐113 and the pre‐infusion plasma renin concentration (PRC), regardless of initial blood pressure or the duration of stenosis. However, the blood pressure fall was not significantly greater in nineteen hypertensive rats than in eleven which remained normotensive. P‐113 did not abolish the hypertension. 3. The extent to which angiotensin II supports blood pressure in rats with renal artery constriction is directly related to the PRC.
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Conscious rats which had undergone unilateral renal artery constriction were infused for 1 h with a specific antagonist of angiotensin II, 1‐Sar‐8‐Ala‐angiotensin II (P‐113). 2. There was a highly significant correlation between the change in blood pressure induced by P‐113 and the pre‐infusion plasma renin concentration (PRC), regardless of initial blood pressure or the duration of stenosis. However, the blood pressure fall was not significantly greater in nineteen hypertensive rats than in eleven which remained normotensive. P‐113 did not abolish the hypertension. 3. 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Conscious rats which had undergone unilateral renal artery constriction were infused for 1 h with a specific antagonist of angiotensin II, 1‐Sar‐8‐Ala‐angiotensin II (P‐113). 2. There was a highly significant correlation between the change in blood pressure induced by P‐113 and the pre‐infusion plasma renin concentration (PRC), regardless of initial blood pressure or the duration of stenosis. However, the blood pressure fall was not significantly greater in nineteen hypertensive rats than in eleven which remained normotensive. P‐113 did not abolish the hypertension. 3. The extent to which angiotensin II supports blood pressure in rats with renal artery constriction is directly related to the PRC.</description><subject>angiotensin antagonist</subject><subject>Angiotensin II - physiology</subject><subject>Animals</subject><subject>Blood Pressure - drug effects</subject><subject>conscious rat</subject><subject>Female</subject><subject>plasma renin concentration</subject><subject>Rats</subject><subject>Renal Artery Obstruction - physiopathology</subject><subject>Renin - blood</subject><subject>Renin - physiology</subject><subject>renin-angiotensin system</subject><subject>renovascular hypertension</subject><subject>Saralasin - pharmacology</subject><issn>0305-1870</issn><issn>1440-1681</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>1976</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNqVkM2OmzAUha2qf-m0b9CF1UV3UBtjwJW6oIwnQSUmAtIqK8sxRkqaTFKcqJm3rxmi7OuFfeVzvnOlA8AnjHzszpetj8MQeThKsI9ZHPmnNUKUhf7lBZjcpJdgggiiHk5i9Ba8s3aLnAtF5A14zWJMKZ2AY1UWHJYPsJlxWHGRCy8V07xsuKhzAetV3fA5dNNsteDV828p4KIq75cZv4ffV3Ap8iJteJUWA-_u1NmqFcxKUTdVnjUD4AKeF6TNe_CqUztrPlzfO7B84E0284pymmdp4ekQUeoFLGKqM6gjXdgqzZI2McZoQoJW05gGqo2pQoxEat0G2pigZTTUVAdrZ8I4IHfg85h77A9_zsae5H5jtdnt1KM5nK1MSBiRKEbO-HU06v5gbW86eew3e9U_SYzk0LbcyqFSOVQqh7bltW15cfDH65bzem_aGzrW6-Rvo_x3szNP_xEsM75gA--N_MaezOXGq_63jGISU_lLTOU8WdTzefxD_iT_ACaYldI</recordid><startdate>19760101</startdate><enddate>19760101</enddate><creator>Oates, Helen F.</creator><general>Blackwell Publishing Ltd</general><scope>BSCLL</scope><scope>CGR</scope><scope>CUY</scope><scope>CVF</scope><scope>ECM</scope><scope>EIF</scope><scope>NPM</scope><scope>AAYXX</scope><scope>CITATION</scope><scope>7X8</scope></search><sort><creationdate>19760101</creationdate><title>ROLE OF THE RENIN-ANGIOTENSIN SYSTEM IN HYPERTENSION PRODUCED BY UNILATERAL RENAL ARTERY CONSTRICTION IN THE RAT</title><author>Oates, Helen F.</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c4055-2969afe0f3f4dac98d8eeec332dc5752ad75a0936abd2cee2d954c5c2bec31123</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>1976</creationdate><topic>angiotensin antagonist</topic><topic>Angiotensin II - physiology</topic><topic>Animals</topic><topic>Blood Pressure - drug effects</topic><topic>conscious rat</topic><topic>Female</topic><topic>plasma renin concentration</topic><topic>Rats</topic><topic>Renal Artery Obstruction - physiopathology</topic><topic>Renin - blood</topic><topic>Renin - physiology</topic><topic>renin-angiotensin system</topic><topic>renovascular hypertension</topic><topic>Saralasin - pharmacology</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Oates, Helen F.</creatorcontrib><collection>Istex</collection><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>MEDLINE - Academic</collection><jtitle>Clinical and experimental pharmacology &amp; physiology</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Oates, Helen F.</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>ROLE OF THE RENIN-ANGIOTENSIN SYSTEM IN HYPERTENSION PRODUCED BY UNILATERAL RENAL ARTERY CONSTRICTION IN THE RAT</atitle><jtitle>Clinical and experimental pharmacology &amp; physiology</jtitle><addtitle>Clin Exp Pharmacol Physiol</addtitle><date>1976-01-01</date><risdate>1976</risdate><volume>3</volume><issue>1</issue><spage>95</spage><epage>98</epage><pages>95-98</pages><issn>0305-1870</issn><eissn>1440-1681</eissn><abstract>SUMMARY 1. Conscious rats which had undergone unilateral renal artery constriction were infused for 1 h with a specific antagonist of angiotensin II, 1‐Sar‐8‐Ala‐angiotensin II (P‐113). 2. There was a highly significant correlation between the change in blood pressure induced by P‐113 and the pre‐infusion plasma renin concentration (PRC), regardless of initial blood pressure or the duration of stenosis. However, the blood pressure fall was not significantly greater in nineteen hypertensive rats than in eleven which remained normotensive. P‐113 did not abolish the hypertension. 3. The extent to which angiotensin II supports blood pressure in rats with renal artery constriction is directly related to the PRC.</abstract><cop>Oxford, UK</cop><pub>Blackwell Publishing Ltd</pub><pmid>971555</pmid><doi>10.1111/j.1440-1681.1976.tb00594.x</doi><tpages>4</tpages></addata></record>
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subjects angiotensin antagonist
Angiotensin II - physiology
Animals
Blood Pressure - drug effects
conscious rat
Female
plasma renin concentration
Rats
Renal Artery Obstruction - physiopathology
Renin - blood
Renin - physiology
renin-angiotensin system
renovascular hypertension
Saralasin - pharmacology
title ROLE OF THE RENIN-ANGIOTENSIN SYSTEM IN HYPERTENSION PRODUCED BY UNILATERAL RENAL ARTERY CONSTRICTION IN THE RAT
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